SLAM (CDw150) is a cellular receptor for measles virus

  title={SLAM (CDw150) is a cellular receptor for measles virus},
  author={Hironobu Tatsuo and Nobuyuki Ono and Kotaro Tanaka and Yusuke Yanagi},
Measles virus continues to be a major killer of children, claiming roughly one million lives a year. Measles virus infection causes profound immunosuppression, which makes measles patients susceptible to secondary infections accounting for high morbidity and mortality. The Edmonston strain of measles virus, and vaccine strains derived from it, use as a cellular receptor human CD46 (refs 3, 4), which is expressed on all nucleated cells; however, most clinical isolates of measles virus cannot use… 

Measles virus receptor SLAM (CD150).

This review is concerned with the identification of a new MV receptor and its implication for understanding the pathology and pathogenesis of MV infection.

The cellular receptor for measles virus—elusive no more

  • Y. Yanagi
  • Biology
    Reviews in medical virology
  • 2001
It is shown that human signalling lymphocytic activation molecule (SLAM; also known as CDw150) is a cellular receptor for measles virus, including the Edmonston strain.

CD147/EMMPRIN Acts as a Functional Entry Receptor for Measles Virus on Epithelial Cells

This is the first report among members of the Mononegavirales that CD147 is used as a virus entry receptor via incorporated CypB in the virions, independently of MeV H.

Tumor Cell Marker PVRL4 (Nectin 4) Is an Epithelial Cell Receptor for Measles Virus

It is demonstrated that wild type measles virus infects primary airway epithelial cells grown in fetal calf serum and many adenocarcinoma cell lines of the lung, breast, and colon and several strains of measles virus were shown to use PVRL4 as a receptor.

CD150 (SLAM) Is a Receptor for Measles Virus but Is Not Involved in Viral Contact-Mediated Proliferation Inhibition

The data indicate that proliferation inhibition induced by MV contact is independent of the presence or absence of the virus-binding receptors SLAM and CD46, and the cell-type-specific expression of SLAM does not correlate with the sensitivity of cells for proliferation inhibition.

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

The findings suggest that the use of SLAM as a cellular receptor may be a property common to most, if not all, morbilliviruses and explain the lymphotropism and immunosuppressive nature of morbillIViruses.

[Two different receptors for wild type measles virus].

Nectin4, a cellular adhesion junction molecule, was identified as the epithelial cell receptor for MV and provides a deep insight into measles pathogenesis.

Induction of the measles virus receptor SLAM (CD150) on monocytes.

Anti-SLAM monoclonal antibodies efficiently blocked infection of activated monocytes with a wild-type strain of MV and indicate that SLAM is readily induced and acts as a monocyte receptor for MV.

Measles Virus Infects both Polarized Epithelial and Immune Cells by Using Distinctive Receptor-Binding Sites on Its Hemagglutinin

The results indicate that MV has an intrinsic ability to infect both polarized epithelial and immune cells by using distinctive receptor-binding sites on the attachment protein corresponding to each of their respective receptors.

Analysis of receptor (CD46, CD150) usage by measles virus.

It is demonstrated that the single amino acid exchange in the haemagglutinin (H) protein at position 481 Asn/Tyr (H481NY) determines whether the virus can utilize CD46, and demonstrates that the binding sites for SLAM and CD46 are distinct.



Clinical Isolates of Measles Virus Use CD46 as a Cellular Receptor

The results indicate that patient isolates that have not been adapted to tissue culture cell lines use CD46 as a receptor, and confirm the relevance of the CD46 receptor to natural measles infection.

Human membrane cofactor protein (CD46) acts as a cellular receptor for measles virus

Results show that the human CD46 molecule serves as an MV receptor allowing virus-cell binding, fusion, and viral replication and open new perspectives in the study of MV pathogenesis.

Marmoset lymphoblastoid cells as a sensitive host for isolation of measles virus

It was suspected that measles virus is subject to host cell-mediated selection and that the viruses grown in B95a cells are more representative of measles virus circulating among humans than are the viruses selected in Vero cells.

Experimental measles. I. Pathogenesis in the normal and the immunized host.

Animals vaccinated with the attenuated Moraten strain did not develop clinical or pathologic signs of measles after challenge, but moderate to marked hyperplasia occurred in the lymph nodes and spleen of a vaccinated animal on Day 7 after pathogenic virus challenge, suggesting that an effective measles vaccine limits but does not prevent infection with wild-type measles virus.

Interaction of measles virus glycoproteins with the surface of uninfected peripheral blood lymphocytes induces immunosuppression in vitro.

It is indicated that a small number of MV-infected PBLs can induce a general nonresponsiveness in uninfected P BLs by surface contact, which may, in turn, account for the general suppression of immune responses observed in patients with acute measles.

A Single Amino Acid Change in the Hemagglutinin Protein of Measles Virus Determines Its Ability To Bind CD46 and Reveals Another Receptor on Marmoset B Cells

Evidence for a measles virus receptor other than CD46 on transformed marmoset and human B cells is provided, through the use of a direct binding assay, that a second receptor for measles virus is present on primate B cells.

Differential downregulation of CD46 by measles virus strains

It is reported that neither the source of MV nor the cell type used for isolation directly influenced the capacity for CD46 modulation of these MV isolates.

Virus Entry Is a Major Determinant of Cell Tropism of Edmonston and Wild-Type Strains of Measles Virus as Revealed by Vesicular Stomatitis Virus Pseudotypes Bearing Their Envelope Proteins

The results indicate that the difference in cell tropism between these MV strains was largely determined by virus entry, in which the H proteins of respective MV strains play a decisive role.

A system for functional analysis of Ebola virus glycoprotein.

It is suggested that cell surface glycoproteins with N-linked oligosaccharide chains contribute to the entry of Ebola viruses, presumably acting as a specific receptor and/or cofactor for virus entry.